Rapid rates during bradycardia prolong ventricular refractoriness and facilitate ventricular tachycardia induction with cesium in dogs.
Rapid rates during bradycardia prolong ventricular refractoriness and facilitate ventricular tachycardia induction with cesium in dogs.
复制标题
心动过缓期间的快速心率可延长犬的心室不应期并促进铯诱发室性心动过速。
DOI：
10.1161/01.cir.94.2.217
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发表时间：
1996
期刊：
影响因子：
37.8
通讯作者：
Zipes,DP
中科院分区：
文献类型：
--
作者：
Satoh,T;Zipes,DP
研究背景心动过缓可促进某些室性心动过速(VTS)的发生。我们调查了相对心动过缓本身或从快速到较慢的心室率的转变是否可能在VT的发生中起重要作用。方法和结果我们研究了通过射频导管消融房室交界处产生房室传导阻滞的麻醉闭胸犬组。其中一组为不间断房室传导阻滞，另一组为快速左心室起搏。然后两组都接受了递增剂量的CSCL，直到导致持续的VT。我们还测量了房室传导阻滞1周或3天、快速起搏(起搏周期长度[PCL]=500或250ms)1小时或30分钟的不同组犬的心室有效不应期(V-ERP)和QT间期。最后，我们通过测试维拉帕米和去自主神经对V-ERP的影响来研究快速起搏对V-ERP的影响。我们发现，CSCL在有快速起搏的狗中比没有起搏的狗引起更大的早期后除极和更多的室性心动过速。在房室传导阻滞1周的犬，快速起搏1h较起搏前V-ERP和QT间期延长。更改持续了至少3个小时。快速起搏仅30min，PCL为250ms，叠加窦性心律，均可延长V-ERP，但延长程度较小。仅3d完全房室传导阻滞和去自主神经不影响快速起搏所产生的V-ERP延长，而维拉帕米显著钝化但不能消除这种延长。结论在相同的PCLS条件下，心动过速合并心动过缓的心脏较单纯心动过缓的心脏表现出更长的V-ERP、QT间期和单相动作电位时程，更容易发生室性心动过速。不应期延长至少3h，Δ事件相关电位受起搏前心率、起搏持续时间和起搏持续时间的影响。这种对快速反应的机制似乎与钙有关，至少部分是这样。
BackgroundBradycardia can promote the development of some ventricular tachycardias (VTs). We investigated whether relative bradycardia per se or the transition from a rapid to a slower ventricular rate might be important in developing VT.Methods and ResultsWe studied groups of anesthetized closed-chest dogs that had AV block produced by radiofrequency catheter ablation of the AV junction. One group had uninterrupted AV block; the other group underwent a period of rapid left ventricular pacing. Both groups then received incremental doses of CsCl until sustained VT resulted. We also measured ventricular effective refractory period (V-ERP) and QT interval in separate groups of dogs that had AV block for 1 week or 3 days with and without rapid pacing (pacing cycle length [PCL]=500 or 250 ms) for 1 hour or 30 minutes. Finally, we investigated the effects of rapid pacing on V-ERP by testing the effects of verapamil and autonomic denervation on these changes. We found that CsCl induced larger early afterdepolarizations and a greater prevalence of VT in dogs with rapid pacing than in dogs without. In dogs that had AV block for 1 week, 1 hour of rapid pacing prolonged V-ERP and QT interval compared with V-ERP and QT interval before pacing. Changes persisted for at least 3 hours. Rapid pacing for only 30 minutes and at a PCL of 250 ms, as well as superimposition on sinus rhythm, each prolonged V-ERP but to a lesser extent. Only 3 days of complete AV block and autonomic denervation did not affect the prolongation of V-ERP produced by rapid pacing, whereas verapamil significantly blunted but did not eliminate the prolongation.ConclusionsAt the same PCLs, the heart exposed to transient tachycardia superimposed on bradycardia exhibited a longer V-ERP, QT interval, and monophasic action potential duration and greater ease for developing VT than the heart exposed only to bradycardia. The prolongation of refractoriness lasted for at least 3 hours, and the Δ-ERP was influenced by the heart rate before pacing, the duration of pacing, and the PCL. The mechanism for this response to rapid rates appears to involve calcium, at least in part.